Cerebrovascular accident after taipan bite

To the Editor: A 14-year-old boy was admitted to Port Moresby General Hospital (PMGH), Papua New Guinea, six hours after being bitten on the left ankle by a snake in Rigo, Central Province. He collapsed minutes after the bite and was semiconscious when seen at the local health centre one hour later. His blood was noted to be non-clotting at this time and he was given one vial of polyvalent antivenom by intravenous infusion and referred to PMGH. On arrival, he was semiconscious and irritable with a coma score of 8.' His blood did not clot and he was bleeding from gums, mouth and venepuncture sites. He had ptosis and reduction of eye movements. He was noted to have reduced power in his left arm. A bite site swab analysed with a Venom Detection Kit (CSL Limited, Parkville, Vic) was strongly positive for taipan venom. Due to a shortage in the hospital, it was not possible to give the patient more antivenom. He was given four units of fresh frozen plasma after which his blood became coagulable. After progression of the neurotoxicity and involvement of both pharyngeal and respiratory musculature, he was intubated and subsequently ventilated for three days. His peripheral strength gradually improved but flaccid paralysis persisted in his left arm and he was noted to have left facial weakness. Later, hemisensory loss affecting the left arm and dyspraxia were found, but there was no apparent visual field defect. The patient absconded on the tenth hospital day, by which time he had regained some power on the left side but still had a marked functional deficit. The venom of the Papuan taipan (Oxyuranus scutellatus canni) contains procoagulants and haemorrhagins. Abnormalities of haemostasis are a cardinal sign of envenoming, and bleeding from cuts, venepuncture sites and gums is common. This patient's signs were consistent with a spontaneous bleed in the territory of the right middle cerebral artery, possibly in association with a predisposing vascular abnormality. Intracranial bleeds have been reported following the bites of other elapid snakes>' and occur occasionally in patients bitten by Papuan taipans (Lalloo & Trevett, unpublished observations). It is interesting to note that this vascular event occurred within 30 minutes of envenoming, before the administration of antivenom. The mechanism could have been intracranial thrombosis occurring during the early, hypercoagulable phase of envenoming. There is a theoretical risk that giving a patient clotting factors before circulating procoagulants have been adequately neutralised by anti venom could exacerbate this problem. Early collapse is not uncommon in victims of taipan bite. The mechanism remains obscure in the majority of cases and most are not associated with persisting neurological deficit. As has been described in patients envenomed by several other elapids, the coagulation abnormalities produced by the venom of the Papuan taipan can cause cerebrovascular accidents. It is possible that this may be a mechanism of some of the sudden early deaths which occur in taipan bite.